Retroviral structural genes generally code for large overlapping polyproteins that are later processed into functional peptide products by virally encoded protease and cellular proteases. The encoding genes of the virus are Figure 388-1 Genomic structure of human T-lymphotropic viruses. This may contribute to the long interval (sometimes many years to decades) between the time of infection and disease. Factors that control viral replication (viral regulatory genes, cell stimulation, and possibly co-infections) may also be cofactors in disease progression. The virus from Melanesia differs molecularly from the Japanese and African strains by 5 to 10%, the result of the independent evolution of the virus in these populations separated for tens of thousands of years. An Asian focus was recently reported in remote areas of Mongolia, among people who share genetic links with Native American populations whose ancestors emigrated from this region during the Ice Age. Infections in Europe occur among injection drug users who may have acquired the virus from contact with U. The third major route of transmission is parenteral, through either transfusion or injection drug use. Health care and laboratory workers who experience a needle stick, skin, or mucous membrane exposure in the absence of protective barriers have little or no risk for infection with a single case of such infection documented after exposure to a "microtransfusion" from a syringe. In the United States, with a low prevalence of infection it is estimated that there are approximately 30 cases per year. The age group of cases ranges from adolescence to a peak in middle-aged (40s in the Caribbean and 50s in Japan) adults. The diagnosis should be considered in an adult with mature T-cell lymphoma and hypercalcemia and/or cutaneous involvement, particularly if the individual is from a known risk group or endemic region. Occasionally, cases are antibody negative but provirus is detectable in the blood or in biopsy specimens. Experimental approaches under investigation include topoisomerase inhibitors, monoclonal antibodies, and interferon and zidovudine. Zidovudine and interferon-alpha induce responses (66%) in cases, but overall survival is poor. This disease is characterized by a chronic, slowly progressive development of spastic paraparesis resulting from the demyelination of the long motor neurons of the spinal cord. Panel A and B display the polylobulated morphology of the acute type, with the highly characteristic "flower cell" shown in panel B. This syndrome differs from classic multiple sclerosis because of its generally slow, progressive course and the absence of a waxing and waning symptomatology and the primary neurologic defect of demyelination of the long motor neurons. Treatment with corticosteroids and immunosuppressive therapies benefit some patients, ranging between 30 and 50% in one series, particularly those with rapidly progressive disease; danazol, and androgenic steroid, improves urinary and fecal incontinence but does not affect the underlying neurologic deficit. Recently, pentoxifylline was reported in an uncontrolled trial to have favorable effects on clinical symptoms and on subclinical immunologic perturbations. In children and adults with this syndrome, patients develop refractory bacterial infections with saprophytic skin organisms that respond to antibiotic therapy but relapse when therapy is stopped. Early in the infection phase, host immune responses to the virus are activated, producing viral antibodies and cytotoxic T cells targeted at viral antigens. The latent period for this process is years to several decades; it involves an interaction between viral expression and oncogenic mutations. For malignancy to develop, additional genetic changes most probably take place. Current data suggest an indirect mechanism of pathogenesis involving immune-mediated responses that appear to cause local damage in the myelin sheath of the long motor neuron. For example, in Japan, epidemiologic data show that new infections are declining because of changing socioeconomic and lifestyle factors, whereas in developing countries rates as high as 1 to 1. They comprise one of the five major subgroups, or genera, of the Picornavirus (pico, small; rna, ribonucleic acid) family. The other Picornavirus genera are: rhinoviruses, which inhabit the upper respiratory tract and include the principal recognized etiologic agents of the common cold (see Chapter 375); cardioviruses, recovered chiefly from rodents and only very rarely implicated in human disease; aphthoviruses, named for the vesicular lesions that they produce in cloven-footed animals; and hepatovirus, a newly designated genus with human hepatitis A virus as its only currently recognized member. Consequently, enteroviruses that have undergone limited replication in the oropharynx survive passage through the stomach and implant in the lower intestinal tract, where they undergo more extensive multiplication. They are further distinguished from enteroviruses by their lower optimal temperature of replication (33° C versus 37° C for enteroviruses) and higher buoyant density in cesium chloride. Because rhinoviruses inhabit the nasopharynx, they have no obvious need for acid stability, and preferential replication at lower than body temperature probably reflects their adaptation to the cooler nasal passages.
West Chair in Cancer Research Cell and Molecular Pharmacology Medical University of South Carolina Charleston, South Carolina Professor of Pathology Weill Medical College of Cornell University Memorial Sloan-Kettering Cancer Center New York, New York Brian B. Tuch, PhD Associate Director, Translational Genomics Onyx Pharmaceuticals South San Francisco, California xxii Contributors Catherine E. Ulbricht, PharmD Founder, Natural Standard Vice President, Integrated Therapeutics & Clinical Solutions Therapeutic Research Center Senior Attending Pharmacist Massachusetts General Hospital Somerville, Massachusetts Thomas S. Weinberg, PhD Professor and Director, Division of Surgical Pathology Department of Pathology University of Illinois Hospital and Health Sciences System University of Illinois College of Medicine Chicago, Illinois Christopher G. Lamborn Chair for Neuro-Oncology Professor of Surgery (Neurosurgery) Cleveland Clinic Lerner College of Medicine of Case Western Reserve University Associate Director, Rose Ella Burkhardt Brain Tumor and Neuro-Oncology Center Cleveland Clinic Cleveland, Ohio Christine M. Gragnani Chair Georgetown University Medical Center Washington, District of Columbia Shelly M. Lee Moffitt Cancer Center and Research Institute Tampa, Florida Certified Genetic Counselor GeneDx Gaithersburg, Maryland Samuel A. Our intention with the first edition was to publish a book that was comprehensive and balanced, covering not just one field, as had been the practice of cancer texts before 1982, but providing in-depth, expert coverage of all the specialties. In fact, a feature of the disease-oriented chapters then and now has been co-authorship by each of the major specialties. Even in the early 1980s, it was apparent the field of cancer was changing rapidly and the regular production of new editions would be necessary to keep information fresh. Ten editions in 32 years has to be some kind of record for textbooks and accounts for the fact that Cancer: Principles & Practice of Oncology is the most popular cancer textbook in the world. With the increase in the rate of new information and the digital information revolution, the text has changed too. For this reason, the 10th edition will be updated quarterly by a team of experts selected by the editors. The new information will be inserted and highlighted in the appropriate chapters, with references, and updates will be posted to the online version. This makes Cancer: Principles & Practice of Oncology the most up-to-date, easily searchable cancer text in the world, and the only comprehensive cancer text that is continuously updated. A perusal of how the contents have evolved from the first edition to the tenth shows the breathtaking pace of change in our understanding of the biology of cancer and the application of this information to the practice of medicine in the past 32 years. All these changes have been chronicled in the 10 editions of the book and the text has been a major vehicle for the translation of new information into practice. Gartner, and Carlos Lуpez-Otin Introduction 2 Cancer Genes and Their Mutations 2 Identification of Cancer Genes 2 Somatic Alteration Classes Detected by Cancer Genome Analysis 10 Pathway-Oriented Models of Cancer Genome Analysis 11 Networks of Cancer Genome Projects 13 the Genomic Landscape of Cancers 15 Integrative Analysis of Cancer Genomics 16 the Cancer Genome and the New Taxonomy of Tumors 16 Cancer Genomics and Drug Resistance 19 Perspectives of Cancer Genome Analysis 20 Acknowledgments 20 5. Weinberg Introduction 24 Hallmark Capabilities, in Essence 24 Two Ubiquitous Characteristics Facilitate the Acquisition of Hallmark Capabilities 33 the Constituent Cell Types of the Tumor Microenvironment 35 Therapeutic Targeting of the Hallmarks of Cancer 41 Conclusion and a Vision for the Future 42 Acknowledgment 43 6. Aggarwal Introduction 83 Molecular Basis of Inflammation 83 Role of Inflammation in Transformation 83 Role of Inflammation in Survival 84 Role of Inflammation in Proliferation 85 Role of Inflammation in Invasion 85 Role of Inflammation in Angiogenesis 85 Role of Inflammation in Metastasis 86 Epigenetic Changes and Inflammation 86 Role of Inflammation in Cancer Diagnosis 87 Inflammation and Genomics 87 Inflammation and Targeted Therapies 87 Conclusions 87 3. Betz Applications of Molecular Diagnostics in Oncology 45 the Clinical Molecular Diagnostics Laboratory: Rules and Regulations 48 Specimen Requirements for Molecular Diagnostics 49 Molecular Diagnostics Testing Process 49 Technologies 50 7. Shields Introduction 89 the Nature of Chemical Carcinogens: Chemistry and Metabolism 89 Animal Model Systems and Chemical Carcinogenesis 90 Molecular Epidemiology, Chemical Carcinogenesis, and Cancer Risk in Human Populations 91 Aristolochic Acid and Urothelial Cancers as a Model for Identifying Human Carcinogens 92 xxix xxx Contents 8. Lawrence Introduction 136 Biologic Aspects of Radiation Oncology 136 Factors that Affect Radiation Response 141 Drugs that Affect Radiation Sensitivity 143 Radiation Physics 144 Treatment Planning 148 Other Treatment Modalities 149 Clinical Applications of Radiation Therapy 151 Treatment Intent 152 Fractionation 153 Adverse Effects 153 Principles of Combining Anticancer Agents with Radiation Therapy 155 9. Willett Introduction 103 Methodologic Challenges 103 the Role of Individual Food and Nutrients in Cancer Etiology 104 Other Foods and Nutrients 108 Dietary Patterns 110 Diet During the Early Phases of Life 110 Diet after a Diagnosis of Cancer 110 Summary 111 Limitations 111 Future Directions 112 Recommendations 112 14. Kochenderfer Introduction 158 Human Tumor Antigens 158 Human Cancer Immunotherapies 161 10. McLeod Introduction 183 Pharmacogenomics of Tumor Response 183 Pharmacogenomics of Chemotherapy Drug Toxicity 186 Conclusions and Future Directions 188 17. Tew Perspectives 189 Chemistry 189 Classification 189 Clinical Pharmacokinetics/Pharmacodynamics 193 Therapeutic Uses 194 Toxicities 195 Complications with High-Dose Alkylating Agent Therapy 196 Alkylating AgentSteroid Conjugates 196 Drug Resistance and Modulation 197 Recent Developments 197 12. Boise Biochemistry of the Ubiquitin-Proteasome Pathway 258 Proteasome Inhibitors 258 Proteasome Inhibitors in Cancer 259 25. Wasif Saif and Edward Chu Antifolates 208 5-Fluoropyrimidines 210 Capecitabine 212 Cytarabine 213 Gemcitabine 214 6-Thiopurines 214 Fludarabine 215 Cladribine 215 Clofarabine 216 26. Deshpande Homoharringtonine and Omacetaxine 267 l-Asparaginase 267 Bleomycin 268 Procarbazine 268 Vismodegib 269 Ado-Trastuzumab Emtansine 269 Sirolimus and Temsirolimus 269 Everolimus 270 Thalidomide, Lenalidomide, and Pomalidomide 270 20. Harris Microtubules 228 Taxanes 228 Vinca Alkaloids 232 Microtubule Antagonists 234 Mitotic Motor Protein Inhibitors 234 Mechanisms of Resistance to Microtubule Inhibitors 235 27.
Systemic paracoccidioidomycosis with central nervous system involvement [in Portuguese]. An uncommon neurologic presentation in the course of paracoccidioidomycosis: report of a case [in Portuguese]. Paracoccidioidomycosis evidencing spinal cord involvement treated with success by fluconazole [in Portuguese]. Brain localization of South American blastomycosis: considerations apropos of 9 cases [in Portuguese]. Differentiation of pyogenic brain abscesses from necrotic glioblastomas with use of susceptibility-weighted imaging. Paracoccidioidomycosis: epidemiological and clinical aspects in 546 cases studied in the state of Espirito Santo, Brazil. Proton magnetic resonance spectroscopy and magnetic resonance imaging findings in a patient with central nervous system paracoccidioidomycosis. No relationship was found between the location of the lesion and clinical symptoms. Lesions did not change in size or signal during a median follow-up of 3 years, suggesting that multinodular and vacuolating posterior fossa lesions of unknown significance are benign malformative lesions that do not require surgical intervention or removal. Voxel placement included both the lesion and normal tissue with a ratio of approximately 80%/20%, respectively. This study was approved by our institutional Research Ethics Board (Fondation Ophtalmologique A. All reading sessions were completed on a dedicated workstation using Horos software (Nimble Co, Annapolis, Maryland). One of these 12 patients had an associated brain stem glioblastoma and was excluded. Demographic features were recorded as well as symptoms prompting imaging and clinical reports, including a comprehensive neurologic examination and follow-up. We calculated 3 indices: choline/creatine, choline/N-acetyl aspartate, and N-acetyl aspartate/creatine. The type of margins between the nodules and the adjacent normal-appearing white matter, defined as sharp or blurred. The presence of a mass effect, defined as any shift in any of the intracranial structures, including ventricles. A size change was defined as positive in the case of a change superior to or equal to 5% of initial size. A signal change was defined as positive in the case of a change of at least 1 component of the signal of the lesion on any of the sequences used, compared with the normal-appearing cerebellar white matter. Almost all lesions centered on the vermis extended laterally to the cerebellar hemispheres: 5/7 (71%). Conversely, none of the lesions centered on a cerebellar hemisphere extended to the vermis (Fig 1). One patient presented with postcontrast enhancement of the nodule of 1 lesion (Fig 2). Note the small mass effect and distortion of the lateral margin of the fourth ventricle. It was missing in images of 2 patients with low-resolution We describe the imaging characteristics of a new entity that we imaging. This sort of evidence might tumor,8-14 which was added in the World Health Organization help rule out differential diagnoses. Classification of Tumors of the Central Nervous System in Two patients had very subtle cortical involvement on imaging, 2016. The second patient had Center of the lesion been taking cyproterone acetate for a Cerebellum long time, which had been reported to Vermis 7/11 64 Left cerebellar hemisphere 1/11 9 increase the chance of developing a Right cerebellar hemisphere 2/11 18 meningioma. Multinodular and vacuolating neuronal tumors of the cerebrum: 10 cases of a distinctive seizureassociated lesion: multinodular and vacuolating neuronal tumors. The 2016 World Health Organization Classification of Tumors of the Central Nervous System: a summary.
In the absence of comparative trials using the same agent with different doses and schedules, superiority of one regimen over the other cannot be assessed. Drugs with little or no activity, especially if they were evaluated prior to 2000, are not included in this table. An antimetabolite, the drug has been used in a variety of schedules and doses in various epithelial malignancies of gastrointestinal origin. One method involved the use of rapid intravenous injections on a weekly basis, or daily for 5 consecutive days. Single-Agent Versus Combination Chemotherapy the potential advantage of giving combination chemotherapy versus single-agent chemotherapy has been evaluated by Wagner et al. In the updated analysis, a test for heterogeneity was not statistically significant; they concluded that this indicated that the results of the different studies were consistent. Not surprisingly, toxicity is higher when several agents are given together, although this was not statistically significant. They also evaluated the role of several different combinations of cytotoxic agents, including anthracyclines as part of combination chemotherapy. In contrast to anthracyclines, there was a more modest, albeit not statistically significant, benefit for irinotecan-containing combinations. The response rate as a secondary objective was 36% for docetaxel-containing regimens versus 31% for nondocetaxel-containing regimens (not statistically significant). Similarly, oxaliplatin regimens were compared to cisplatin-containing regimens with modest superiority to oxaliplatin. Like capecitabine, S-1 is now undergoing study in combination with other agents, particularly cisplatin. The data available suggest similar activity as seen with other oral fluorinated pyrimidines. In both previously treated and untreated patients, a response rate of approximately 15% was reported. The major toxicities for cisplatin are nausea and vomiting, peripheral neuropathy, ototoxicity, and nephropathy. The development of efficacious antiemetics has significantly improved control of nausea and vomiting. An analogue of cisplatin, carboplatin, has been less well studied in gastric cancer; it appears to have less activity in this disease, as compared to other epithelial malignancies. Most recently, oxaliplatin, a diamino cyclohexane extensively used in the treatment of colorectal cancer, was included as part of combination chemotherapy for gastric cancer. Both paclitaxel and docetaxel have been studied as single agents in gastroesophageal cancers. Patients may have received prior treatment, and 262 patients were evaluable for Practice of oncology response. A schedule using lower doses given once weekly has also been studied with similar activity. Paclitaxel has also been studied in gastric cancer, although in smaller numbers of patients, and has a similar degree of cytotoxic activity. It has been studied both as a single agent and in combination with other cytotoxic agents. When used alone, response rates of 15% to 25% have been reported in both previously treated and untreated patients with advanced gastric cancer. They concluded that irinotecan-containing multidrug chemotherapy combinations had a modest survival benefit, which was not statistically significant, when compared with regimens not including irinotecan. Single-agent data from the 1960s and 1970s show a response rate for doxorubicin of 17%, and for epirubicin a similar response rate of approximately 19%. The anthracyclines have undergone more extensive study in combination chemotherapy for advanced gastric cancer. The response rates range from 10% to 25%, and the median duration of response is relatively short (4 to 6 months). Like other malignancies, multidrug regimens using agents that have single-agent activity have been extensively studied in gastric cancer. The recent Cochrane review summarizing a comparison of different regimens including three-drug versus two-drug combinations has already been discussed. Major objective tumor regression was reported in 20% to 30% of patients; complete clinical remission was very uncommon, however.
Noise or tactile stimuli may precipitate spasms and generalized convulsions, although they occur spontaneously as well. Involvement of the autonomic nervous system may result in severe arrhythmias, oscillation in the blood pressure, profound diaphoresis, hyperthermia, rhabdomyolysis, laryngeal spasm, and urinary retention. Complications include fractures from sustained contractions and convulsions, pulmonary emboli, bacterial infections, and dehydration. Localized tetanus refers to involvement of the extremity with a contaminated wound and shows considerable variation in severity. In more severe cases there are intense, painful spasms that usually progress to generalized tetanus. This is a relatively unusual form of tetanus, and the prognosis for survival is excellent. The clinical symptoms consist of isolated or combined dysfunction of the cranial motor nerves, most frequently the seventh cranial nerve. The usual cause is the use of contaminated materials to sever or dress the umbilical cord in newborns of unimmunized mothers. The child typically shows irritability, facial grimacing, and severe spasms with touch. Cerebrospinal fluid analysis is entirely normal, and the electroencephalogram generally shows a sleep pattern. Diagnostic testing is usually not necessary except in cases lacking an identified portal of entry. Strychnine also antagonizes glycine, and strychine poisoning is the only condition that truly mimics tetanus. Patients with tetanus require intensive care with particular attention to respiratory support, benzodiazepines, autonomic nervous system support, passive and active immunization, surgical debridement, and antibiotics directed against C. There may be clinical progression for about 2 weeks despite antitoxin treatment because of the time required to complete transport 1676 of toxin. Disease severity may be reduced by partial immunity so that some patients have mild disease with minimal mortality and others show mortality rates as high as 60% despite expert care. Many patients will require endotracheal intubation with benzodiazepine sedation and neuromuscular blockade; a tracheostomy should be placed if the endotracheal tube causes spasms. Benzodiazepines have become the mainstay of therapy to control spasms and provide sedation. The most extensively studied is diazepam given in 5-mg increments; lorazepam or midazolam are equally effective. Tetanus patients may have high tolerance for the sedation effects of these drugs, requiring exceptionally high doses. When tetanus symptoms resolve, the drugs must be tapered over at least 2 weeks to prevent withdrawal reactions. If control of spasms cannot be achieved by benzodiazepines, long-term neuromuscular blockade is performed with vecuronium (6-8 mg/hour). Equine tetanus immunoglobulin is equally effective, but the rate of allergic reactions is high, owing to the equine source. This preparation should no longer be used except in underdeveloped countries where cost dictates such medical decisions. The standard three-dose schedule of immunization with tetanus toxoid should be given using an injection site separate from that used for immunoglobulin. This generally reflects excessive catecholamine release and is usually treated with labetalol (0. Other treatments for hypertension include morphine by continuous infusion, magnesium sulfate infusion, or an epidural blockade of the renal nerves. The overall mortality rate for generalized tetanus is 20-25 per cent even in modern medical facilities with extensive resources. Patients with moderate or severe generalized tetanus generally require 3 to 6 weeks for recovery. The most frequent cause of death is pneumonia, but many patients have no obvious findings at autopsy, suggesting that death was directly due to the neurotoxin. Nearly all cases of tetanus occur in unimmunized or inadequately immunized individuals.
Sharon Fruit (Japanese Persimmon). Nitroglycerin.
Source: http://www.rxlist.com/script/main/art.asp?articlekey=97060
Nearly 70% of patients had symptoms of cough, chest pain, or superior vena cava syndrome. Ectopic thymic tissue has been found to be widely distributed throughout the mediastinum and neck, particularly the aortopulmonary window and retrocarinal area, and often is indistinguishable from mediastinal fat. Thymomas grossly are lobulated, firm, tan-pink to gray tumors that may contain cystic spaces, calcification, or hemorrhage. They may be encapsulated, adherent to surrounding structures, or frankly invasive. Microscopically, thymomas arise from thymic epithelial cells, although thymocytes or lymphocytes may predominate histologically. True thymomas contain cytologically bland cells and should be distinguished from thymic carcinomas, which have malignant cytologic characteristics. Originally, in 1976, Rosai and Levine11 proposed that thymomas be divided into three types: lymphocytic, epithelial, or mixed (lymphoepithelial). In 1985, Marino and Muller-Hermelink12 proposed a histologic classification system determined by the thymic site of origin-that is, cortical thymomas, medullary thymomas, and mixed thymomas-which were later subdivided further. Currently, the terms noninvasive and invasive thymoma are preferred over benign and malignant designations. Noninvasive thymomas have an intact capsule, are mobile, and are easily resected, although they can be adherent to adjacent organs. In contrast, invasive thymomas invade surrounding structures and should be removed with en bloc resection of involved structures despite a benign cytologic appearance. Metastatic disease may occur in both noninvasive and invasive thymomas and is most commonly seen as pleural implants or pulmonary nodules. Metastases to extrathoracic sites, such as the liver, brain, bone, and kidney, rarely occur. Although lymphomas, carcinoid tumors, and germ-cell tumors all may arise within the thymus, only thymomas, thymic carcinomas, and thymolipomas arise from true thymic elements. Lymphoid cells arrive during week 9 and are separated from the perivascular spaces by a flat epithelial cell layer that creates the bloodthymus barrier. Maturation and differentiation occurs in this antigen-free environment and, during the 4th fetal month, lymphocytes begin to circulate to peripheral lymphoid tissue. These cells have an ectodermal origin and are displaced into the thymic medulla, where they hypertrophy, form tonofilaments, and finally appear as concentric cells without nuclei. Low-grade tumors include squamous cell carcinoma, mucoepidermoid carcinoma, and basaloid carcinoma. High-grade neoplasms include lymphoepitheliomalike carcinoma and small-cell, undifferentiated, sarcomatoid, and clear-cell carcinomas. For instance, low-grade tumors may have Diagnosis A meticulous history and physical examination, along with serologic and imaging studies, usually suggests the diagnosis. Although most anterior mediastinal masses are thymic malignancies, other etiologies also exist (Table 43. An improved pathologic analysis of image-guided percutaneous core needle biopsy specimens makes surgical biopsy rarely necessary. Symptoms and Signs Approximately 40% of mediastinal masses are asymptomatic and discovered incidentally on routine chest imaging. Asymptomatic patients are more likely to have benign lesions, whereas symptomatic patients more often harbor malignancies. Superior vena cava syndrome, Horner syndrome, hoarseness, and neurologic deficits are less common and often signal a malignancy. Microscopic invasion into capsule Macroscopic invasion into neighboring organs (pericardium, great vessels, lung) a. Ocular symptoms are the most frequent initial complaint, eventually progressing to generalized weakness in 80% of cases. Defects in both cellular and humoral immunity have been described, and many patients also have red cell hypoplasia. Radiographic Imaging Studies Imaging studies initially localize mediastinal neoplasms. Red Cell Aplasia Pure red cell aplasia, an autoimmune disorder, occurs in 5% of patients with thymomas. A bone marrow examination reveals an absence of erythroid precursors and, in 30% of cases, a poorly understood associated decrease in platelet and leukocyte numbers. For patients with recurrent disease, octreotide and prednisone were effective in case reports.
Once the endoscope passes into the esophagus, assist the patient into the left lateral position. The esophagus, stomach, and duodenum are visually examined as the endoscope passes through each section. Tissue samples are obtained by inserting a cytology brush or biopsy forceps through the endoscope. When the examination and tissue removal are complete, the endoscope and suction device are withdrawn and the tooth guard and bite block are removed. Instruct the patient to report any chest pain, upper abdominal pain, pain on swallowing, difficulty breathing, or expectoration of blood. This test assists in confirming a diagnosis of cancer found on x-ray or ultrasound or to diagnose certain inflammatory or immunological conditions. Biopsy specimen is usually obtained either percutaneously or after surgical incision. Inform the patient that the test is used to establish a diagnosis of kidney disease. Address concerns about pain and explain that a sedative and/or analgesia will be administered to promote relaxation and reduce discomfort prior to the percutaneous biopsy; a general anesthesia will be administered prior to the open biopsy. The surgical procedure usually takes about 60 min to complete, and sutures may be necessary to close the site. Positively identify the patient, and label the appropriate collection containers with the corresponding patient demographics, date and time of collection, and site location, especially left or right kidney. Open Biopsy: After administration of general anesthesia and surgical prep are completed, an incision is made, suspicious area(s) are located, and tissue samples are collected. Needle Biopsy: A sandbag may be placed under the abdomen to aid in moving the kidneys to the desired position. Direct the patient to take slow deep breaths when the local anesthetic is injected. Instruct the patient to take a deep breathe, exhale forcefully, and hold the breathe while the biopsy needle is inserted and rotated to obtain a core of renal tissue. Pressure is applied to the site for 5 to 20 min, then a sterile pressure dressing is applied. Instruct the patient to immediately report symptoms such as backache, flank pain, shoulder pain, lightheadedness, burning on urination, hematuria, chills, or fever, which may indicate the presence of infection, hemorrhage, or inadvertent puncture of other internal organs. Observe the patient for other signs of distress, including hypotension and tachycardia. Instruct the patient to report any changes in urinary pattern or volume or any unusual appearance of the urine. If urinary volume is less than 200 mL in the first 8 hr, encourage the patient to increase fluid intake unless contraindicated by another medical condition. Inform the patient of a follow-up appointment for removal of sutures, if Access additional resources at davisplus. Refer to the Genitourinary and Immune System tables at the back of the book for related tests by body system. This test is used to assist in confirming a diagnosis of cancer or certain disorders of the hepatic parenchyma. Inform the patient that the test is used to establish a diagnosis of liver disease. Include a list of known allergens, especially allergies or sensitivities to latex or anesthetics. The surgical procedure usually takes about 90 min to complete, and sutures may be necessary to close the site. Open Biopsy: Instruct the patient that nothing should be taken by mouth for 6 to 8 hr prior to a general anesthetic. General: Make sure a written and informed consent has been signed prior to the Access additional resources at davisplus. Assist the patient to the desired position depending on the test site to be used and direct the patient to breathe normally during the beginning of the general anesthetic. Instruct the patient to avoid coughing or straining, as this may increase intra-abdominal pressure.
It is not necessary to clean furniture or carpets, but bed covers, pillow cases, sheets, outer clothes, and underwear if used in the previous 48 hours should be put in a hot water cycle or dry cleaned. In the hospital, patients should have contact isolation for 24 hours after the start of therapy. Particular care should be taken for patients with Norwegian scabies since it is highly contagious, and these patients should be isolated. Dust mites do not bite, but exposure to them may result in rhinitis, asthma, and childhood eczema. Louis encephalitis and western equine encephalitis have been isolated from the chicken mite Dermanyssus gallinae. These mites penetrate the superficial epithelium and cause a papulovesicular or urticarial eruption. The best known of the non-scabies mites is the harvest mite, chigger, or "red bug. They are bright orange to red and attach where clothing fits snugly, especially at the ankles, groin, and waist. Some patients experience a papular, urticarial, or vesicular rash, occasionally with fever and adenopathy. Treatment is a warm soapy bath or shower plus antipruritic lotions; topical corticosteroids or anesthetic ointments are also used. These mites are the vector for Rickettsia tsutsugamushi (scrub typhus) in Central and Eastern Asia. An important mite associated with rats is Ornithonyssus bacoti, a vector of murine or endemic typhus (Rickettsia typhi). Another medically important vector is Liponyssoides sanguineus, the mouse mite, which transmits rickettsialpox (Rickettsia akari) to humans. They do not burrow, but live on the keratin layer of the epidermis, producing a mange-like dermatitis in the animal. Humans, often pet owners, experience transient pruritus and a rash, typically papulovesicles on the flexor side of the arms, breasts, or abdomen. Ticks cause disease in a variety of ways: They transmit microorganisms that cause infection; they cause toxic and hypersensitivity reactions to their salivary secretions; and they directly inject toxin into a human host. Local swelling and erythema may result, and occasionally blistering or ecchymosis follows, sometimes followed by necrosis and ulceration. For Lyme disease, the tick needs at least 24 hours of feeding and possibly 72 hours to transmit disease efficiently. Thus, a tick removed 1997 while it is still wandering in search of a location for feeding or before it has had an adequate chance to feed is not likely to have spread disease to its human host. In North America there are six species that have been identified, including the species that also cause Lyme disease, tularemia, Rocky Mountain spotted fever, ehrlichiosis, Colorado tick fever, and babesiosis. These unilateral localized presentations are attributed to the nearby location of the tick. It is important to consider tick paralysis in a susceptible host; without removal the process may be fatal, but after the tick is removed most patients improve within a few hours. The best ways to prevent tick attachment are to keep pant legs tucked in boots or socks and to use an effective repellent. Approximately 50 species bite humans but only 4 cause severe disease in the United States: the widow (Latrodectus), the brown recluse (Loxosceles), the hobo spider or aggressive house spider (Tegenaria), and the yellow sac spider (Cheiracanthium), a greenish-gray garden dweller that is the most common domestic spider in many areas of the United States. Local treatment requires washing the area, applying cold compresses, and administering tetanus prophylaxis. The brown recluse is not aggressive but hides in clothing and in the bathroom, attic, and closets. Redness, swelling, and tenderness develop; slough, ulceration, and scabbing may follow. Some lesions show central blistering with ecchymosis surrounded by blanched skin, which in turn is surrounded by erythema. This is followed by sweating, nausea, tremor, myalgias, muscle spasm, board-like abdomen, chest pain, paralysis, bradycardia, seizures, and rarely death. There is a red-orange hourglass on the ventral side of the abdomen; however, some species have red markings on the dorsal side, and in some the hourglass is incomplete, appearing more like hatch marks. Systemic therapy is undertaken with intravenous calcium gluconate, muscle relaxants, and tetanus toxoid. Systemic signs may be neurologic (coma, tremor, paralysis of respiratory muscles, seizures), cardiac (hypertension, arrhythmias, pulmonary edema), and pancreatic (scorpion bite is a common cause of pancreatitis in Brazil).
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